该研究旨在研究铜暴露(0、51.3、164、513、1,640和5,130μg/L)对鱼类生长性能的影响。组织学,氧化应激,炎症,大嘴鲈鱼(Micropterussalmoides)幼鱼的凋亡。将270条鱼(2.69±0.02g)随机分为6组鱼缸,每组4周,每组包含三个重复的鱼缸。结果表明,1,640和5,130μg/LCu对鱼类生长和成活率有显著影响(P<0.05)。与对照相比,在513μg/L以上的鱼表现出的组织病理学损害,如较短的初级和次级薄片,较小的肝细胞核,和肝脏中坏死细胞数量的增加。与对照相比,1,640μg/LCu以上的鱼的丙二醛含量明显较高,总超氧化物歧化酶活性水平较低,谷胱甘肽过氧化物酶,和过氧化氢酶在ill和肝脏中(P<0.05)。此外,高浓度Cu(1,640和5,130μg/L)通过上调白介素-1β和肿瘤坏死因子α的表达而显著增加肝脏炎症,并通过增加半胱氨酸天冬氨酸特异性蛋白酶3(caspase-3)和caspase-9的表达而增加肝细胞凋亡(P<0.05)。Pearson相关分析表明,鱼类生长和存活与组织学和抗氧化防御参数呈正相关,与氧化应激参数呈负相关,肝脏炎症,和肝细胞凋亡。一起来看,这些结果表明,高水平的水性铜可以通过损害肝脏和g健康而导致生长迟缓和死亡。
The study aimed to investigate the effect of Cu exposure (0, 51.3, 164, 513, 1,640, and 5,130 μg/L) on fish growth performance, histology, oxidative stress, inflammation, and apoptosis in largemouth bass (Micropterus salmoides) juveniles. 270 fish (2.69 ± 0.02 g) were randomly divided into 6 groups of tanks for 4 weeks with each group comprising three replicate tanks. The results showed that fish exposed to 1,640 and 5,130 μg/L Cu exhibited a significant reduction in fish growth and survival rate (P < 0.05). Compared to the control, the fish at and above 513 μg/L Cu demonstrated histopathological damages in the gills and liver, such as shorter primary and secondary lamellae, smaller hepatocyte nuclei, and an increase in the number of necrotic cells in the liver. Compared to the control, fish at and above 1,640 μg/L Cu had a significantly higher malondialdehyde content and lower activity levels of total superoxide dismutase, glutathione peroxidase, and catalase in the gills and liver (P < 0.05). Furthermore, high concentrations of Cu (1,640 and 5,130 μg/L) significantly increased hepatic inflammation by upregulating interleukin-1β and tumor necrosis factor α expression and hepatic apoptosis by increasing cysteinyl aspartate specific protease 3 (caspase-3) and caspase-9 expression (P < 0.05). Pearson correlation analysis showed that fish growth and survival positively correlated with histological and antioxidant defense parameters, and negatively correlated with oxidative stress parameters, hepatic inflammation, and hepatic apoptosis. Taken together, these results suggest that high levels of waterborne Cu can induce growth retardation and mortality by damaging the liver and gill health.